About Dr. Tony Talebi

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The lifetime risk of ovarian cancer in the general population of women is 1.4 percent and the age-adjusted incidence rate is 12.9 cases per 100,000 women.

The incidence of ovarian cancer varies according to geographical location. Western countries, including the United States, have rates approximately three to seven-fold greater than Japan, although the rate is higher in Japanese immigrants to the United States.

The mean age at diagnosis of ovarian cancer is younger among women with a hereditary ovarian cancer syndrome (BRCA or Lynch syndrome).

RISK FACTORSof Ovarian Cancer — The pathogenetic mechanism(s) that explains the link between many of the risk factors and development of ovarian cancer have not been determined. Two main hypotheses that have been proposed are:

·Repeated ovulation results in repeated minor trauma to the ovarian epithelium, which, in turn, can lead to malignant transformation. Support for this hypothesis is derived from the observation that women with periodic suppression of ovulation as a result of oral contraceptive use, pregnancy, or lactation have a lower incidence of ovarian cancer.

·Persistent ovarian exposure to gonadotropins and elevated estradiol concentrations may be carcinogenic. This hypothesis is supported by the observation that experimentally induced ovarian tumors contain gonadotropin receptors and estrogen can stimulate cell proliferation in cells containing estrogen receptors.

Reproductive and hormonal factors — Reproductive factors appear to play a role in the incidence of ovarian carcinogenesis. The risk of ovarian cancer appears to be increased by infertility, and reduced by oral contraceptive pills and multiparity.

Early menarche or late menopause — Early age of menarche (before age 12) or late age of menopause (after age 50) are associated with increased risk of ovarian cancer.

Nulligravidity — Epidemiologic data suggest a protective effect of multiparity on the risk of EOC; and nulligravidity is a risk factor for the disease

Infertility — Infertility is a risk factor for ovarian cancer, but infertility treatment probably is not. The apparent association between fertility drug use and EOC appears to be related to the fact that infertile women are likely to have used ovulation-stimulating agents as part of their infertility treatment. However, all of the epidemiological studies in this area have methodological issues, such as lack of information on confounders and short follow-up.

Breast ovarian cancer syndrome (BRCA mutations) — BRCA mutations may account for as many as 90 percent of hereditary ovarian cancers, and approximately 10 percent of all ovarian cancers. The risk of ovarian cancer associated with BRCA mutations is discussed in detail separately.

Lynch syndrome — Lynch syndrome (hereditary nonpolyposis colorectal cancer; HNPCC) is associated with other cancers, in particular, endometrial, ovarian, urogenital, and other gastrointestinal primaries. Colorectal cancer is the hallmark disease for HNPCC; endometrial cancer is the second most common malignancy in affected women (occurring in 22 to 60 percent), but ovarian cancer is also increased in frequency (cumulative lifetime risk 9 to 12 percent). HNPCC carriers account for 1 percent of ovarian cancers.

Laboratory Evaluation:

CA 125 tumor marker — The preoperative evaluation of a woman with suspected ovarian cancer includes measurement of the serum glycoprotein CA 125. The serum CA 125 is elevated (≥35 units/mL) in over 80 percent of women with advanced EOC. Such a finding in a postmenopausal woman with a pelvic or abdominal mass should prompt consultation with a gynecologic oncologist.

Treatment of Ovarian Cancer:

The initial management of women with ovarian cancer is surgery.Consultation by a gynecologic oncologist is crucial.Primary surgical cytoreduction followed by systemic chemotherapy is the preferred initial management for women with stage III or IV EOC. There are three exceptions to an initial surgical approach to management.Surgery is performed in women with suspected ovarian cancer to obtain tissue to confirm the diagnosis, assess the extent of disease (staging), and attempt to remove as much of the gross tumor as possible, which is crucial for successful treatment.

·The Gynecologic Oncology Group defines optimal cytoreduction as leaving residual disease less than 1 cm in maximum tumor diameter. The volume of residual disease remaining after cytoreductive surgery inversely correlates with survival; therefore, if it is technically feasible, all visible tumor should be resected at the initial surgical procedure.

·We recommend that cytoreduction be performed by gynecologic oncologists experienced in this surgery since achieving optimal cytoreduction depends, in part, on the judgment, experience, and aggressiveness of the surgeon.

·If the initial surgical attempt at cytoreduction was not optimal and was not a maximal surgical effort, then chemotherapy and secondary surgical cytoreduction may be beneficial, but survival is not as high as with optimal cytoreduction at primary surgery

Stage III and IV disease not optimally cytoreduced — Based upon its favorable safety profile, the survival benefits of paclitaxel-containing as compared to a nonpaclitaxel-containing regimen, and trials supporting the equivalent efficacy of carboplatin and cisplatin, we suggest initial surgery followed by six cycles of intravenous carboplatin plus paclitaxel for women with nonbulky stage IV or suboptimally debulked (residual disease ≥1 cm) stage III EOC.